You are not logged in.

Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity

Chen, Minghui Jessica, Peng, Zhao Feng, Manikandan, Jayapal, Melendez, Alirio J., Tan, Gek San, Chung, Ching Ming, Li, Qiu-Tian, Tan, Theresa M., Deng, Lih Wen, Whiteman, Matthew, Beart, Philip M., Moore, Phillip K. and Cheung, Nam Sang 2011, Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity, Journal of cellular physiology, vol. 226, no. 5, pp. 1308-1322, doi: 10.1002/jcp.22459.

Attached Files
Name Description MIMEType Size Downloads

Title Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity
Author(s) Chen, Minghui Jessica
Peng, Zhao Feng
Manikandan, Jayapal
Melendez, Alirio J.
Tan, Gek San
Chung, Ching Ming
Li, Qiu-Tian
Tan, Theresa M.
Deng, Lih Wen
Whiteman, Matthew
Beart, Philip M.
Moore, Phillip K.
Cheung, Nam SangORCID iD for Cheung, Nam Sang orcid.org/0000-0001-9453-2523
Journal name Journal of cellular physiology
Volume number 226
Issue number 5
Start page 1308
End page 1322
Total pages 15
Publisher John Wiley & Sons
Place of publication Hoboken, United States
Publication date 2011-05
ISSN 0021-9541
1097-4652
Summary Recently the role of hydrogen sulphide (H2S) as a gasotransmitter stimulated wide interest owing to its involvement in Alzheimer's disease and ischemic stroke. Previously we demonstrated the importance of functional ionotropic glutamate receptors (GluRs) by neurons is critical for H2S-mediated dose- and time-dependent injury. Moreover N-methyl-D-aspartate receptor (NMDAR) antagonists abolished the consequences of H2S-induced neuronal death. This study focuses on deciphering the downstream effects activation of NMDAR on H2S-mediated neuronal injury by analyzing the time-course of global gene profiling (5, 15, and 24 h) to provide a comprehensive description of the recruitment of NMDAR-mediated signaling. Microarray analyses were performed on RNA from cultured mouse primary cortical neurons treated with 200 µM sodium hydrosulphide (NaHS) or NMDA over a time-course of 5–24 h. Data were validated via real-time PCR, western blotting, and global proteomic analysis. A substantial overlap of 1649 genes, accounting for over 80% of NMDA global gene profile present in that of H2S and over 50% vice versa, was observed. Within these commonly occurring genes, the percentage of transcriptional consistency at each time-point ranged from 81 to 97%. Gene families involved included those related to cell death, endoplasmic reticulum stress, calcium homeostasis, cell cycle, heat shock proteins, and chaperones. Examination of genes exclusive to H2S-mediated injury (43%) revealed extensive dysfunction of the ubiquitin-proteasome system. These data form a foundation for the development of screening platforms and define targets for intervention in H2S neuropathologies where NMDAR-activated signaling cascades played a substantial role. J. Cell. Physiol. 226: 1308–1322, 2011.
Language eng
DOI 10.1002/jcp.22459
Field of Research 111601 Cell Physiology
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2010, Wiley-Liss, Inc.
Persistent URL http://hdl.handle.net/10536/DRO/DU:30040514

Document type: Journal Article
Collection: School of Medicine
Connect to link resolver
 
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 15 times in TR Web of Science
Scopus Citation Count Cited 16 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 237 Abstract Views, 5 File Downloads  -  Detailed Statistics
Created: Mon, 05 Dec 2011, 12:44:00 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.